Towner R A, Smith N, Saunders D, Carrizales J, Lupu F, Silasi-Mansat R, Ehrenshaft M, Mason R P
Advanced Magnetic Resonance Center, Oklahoma Medical Research Foundation , Oklahoma City, OK , USA.
Free Radic Res. 2015;49(9):1140-6. doi: 10.3109/10715762.2015.1050587. Epub 2015 Jun 1.
Free radicals contribute to the pathogenesis of diabetic cardiomyopathy. We present a method for in vivo observation of free radical events within murine diabetic cardiomyopathy. This study reports on in vivo imaging of protein/lipid radicals using molecular MRI (mMRI) and immuno-spin trapping (IST) in diabetic cardiac muscle. To detect free radicals in diabetic cardiomyopathy, streptozotocin (STZ)-exposed mice were given 5,5-dimethyl-pyrroline-N-oxide (DMPO) and administered an anti-DMPO probe (biotin-anti-DMPO antibody-albumin-Gd-DTPA). For controls, non-diabetic mice were given DMPO (non-disease control), and administered an anti-DMPO probe; or diabetic mice were given DMPO but administered a non-specific IgG contrast agent instead of the anti-DMPO probe. DMPO administration started at 7 weeks following STZ treatment for 5 days, and the anti-DMPO probe was administered at 8 weeks for MRI detection. MRI was used to detect a significant increase (p < 0.001) in MRI signal intensity (SI) from anti-DMPO nitrone adducts in diabetic murine left-ventricular (LV) cardiac tissue, compared to controls. Regional increases in MR SI in the LV were found in the apical and upper-left areas (p < 0.01 for both), compared to controls. The biotin moiety of the anti-DMPO probe was targeted with fluorescently-labeled streptavidin to locate the anti-DMPO probe in excised cardiac tissues, which indicated elevated fluorescence only in cardiac muscle of mice administered the anti-DMPO probe. Oxidized lipids and proteins were also found to be significantly elevated (p < 0.05 for both) in diabetic cardiac muscle compared to controls. It can be concluded that diabetic mice have more heterogeneously distributed radicals in cardiac tissue than non-diabetic mice.
自由基参与糖尿病性心肌病的发病机制。我们提出了一种在小鼠糖尿病性心肌病体内观察自由基事件的方法。本研究报告了使用分子磁共振成像(mMRI)和免疫自旋捕获(IST)对糖尿病心肌中的蛋白质/脂质自由基进行体内成像。为了检测糖尿病性心肌病中的自由基,给链脲佐菌素(STZ)处理的小鼠注射5,5-二甲基-吡咯啉-N-氧化物(DMPO),并给予抗DMPO探针(生物素-抗DMPO抗体-白蛋白-钆-二乙三胺五乙酸)。作为对照,给非糖尿病小鼠注射DMPO(非疾病对照)并给予抗DMPO探针;或者给糖尿病小鼠注射DMPO,但给予非特异性IgG造影剂而非抗DMPO探针。DMPO给药在STZ治疗5天后的第7周开始,抗DMPO探针在第8周给药用于磁共振成像检测。与对照组相比,磁共振成像用于检测糖尿病小鼠左心室(LV)心脏组织中抗DMPO硝酮加合物的磁共振信号强度(SI)显著增加(p < 0.001)。与对照组相比,在LV的顶端和左上方区域发现磁共振SI区域增加(两者均p < 0.01)。抗DMPO探针的生物素部分用荧光标记的链霉亲和素靶向,以在切除的心脏组织中定位抗DMPO探针,这表明仅在给予抗DMPO探针的小鼠心肌中荧光升高。与对照组相比,糖尿病心肌中氧化脂质和蛋白质也显著升高(两者均p < 0.05)。可以得出结论,与非糖尿病小鼠相比,糖尿病小鼠心脏组织中的自由基分布更不均匀。